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钙离子和氯离子流入表皮角质形成细胞可调节表皮板层小体的胞吐作用和皮肤渗透屏障的稳态。

Influx of calcium and chloride ions into epidermal keratinocytes regulates exocytosis of epidermal lamellar bodies and skin permeability barrier homeostasis.

作者信息

Denda Mitsuhiro, Fuziwara Shigeyoshi, Inoue Kaori

机构信息

Shiseido Research Center, Fukuura, Kanazawa-ku, Yokohama, Japan.

出版信息

J Invest Dermatol. 2003 Aug;121(2):362-7. doi: 10.1046/j.1523-1747.2003.12367.x.

DOI:10.1046/j.1523-1747.2003.12367.x
PMID:12880429
Abstract

In the nervous system, influx of calcium and chloride ions into neurons regulates the signaling system by excitation and inhibition, respectively. In this study, we demonstrated the effects of the ion influx into epidermal keratinocytes in the permeability barrier repair process of the skin after damage. Topical application of the neurotransmitters glutamate and nicotine, which activate the calcium channel in neurons, delayed the barrier repair after tape stripping. In contrast, the neurotransmitters GABA and glycine, which activate the chloride channel in neurons, accelerated barrier repair. Topical application of the calcium ionophore ionomycin delayed barrier recovery and chloride ionophore 1 accelerated barrier repair after barrier disruption by tape stripping and acetone treatment. Ionomycin increased the intracellular calcium concentration in cultured keratinocytes whereas the chloride ionophore 1 increased the intracellular chloride ion concentration. In vivo light microscopy and electron microscopy observation showed acceleration of the exocytosis of lipid-containing lamellar bodies by the chloride ionophore and delay of the exocytosis by the calcium ionophore. These results suggest that, like the nervous system, influx of calcium and chloride ions into epidermal keratinocytes through ionotropic receptors plays a crucial role in cutaneous barrier homeostasis.

摘要

在神经系统中,钙离子和氯离子流入神经元分别通过兴奋和抑制来调节信号系统。在本研究中,我们证明了离子流入对皮肤损伤后通透性屏障修复过程中表皮角质形成细胞的影响。局部应用能激活神经元钙通道的神经递质谷氨酸和尼古丁,会延迟胶带剥离后的屏障修复。相反,能激活神经元氯通道的神经递质γ-氨基丁酸(GABA)和甘氨酸则加速了屏障修复。在胶带剥离和丙酮处理破坏屏障后,局部应用钙离子载体离子霉素会延迟屏障恢复,而氯离子载体1则加速屏障修复。离子霉素增加了培养角质形成细胞内的钙浓度,而氯离子载体1增加了细胞内的氯浓度。体内光学显微镜和电子显微镜观察显示,氯离子载体可加速含脂质板层小体的胞吐作用,而钙离子载体则延迟胞吐作用。这些结果表明,与神经系统一样,通过离子型受体使钙离子和氯离子流入表皮角质形成细胞在皮肤屏障稳态中起关键作用。

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